Pubmed (TDAH) du 24/10/26
1. Adamou M, Hill D. De-diagnosis and the problem of revisability in adult ADHD and autism. Front Sociol. 2026; 11: 1944117.
Recorded diagnoses of attention-deficit/hyperactivity disorder (ADHD) and autism in adults have risen sharply across high-income health systems, and demand for assessment has risen faster still, while the best available population estimates of prevalence appear to have moved comparatively little. This paper treats that divergence as an analytic problem. We argue that adult neurodevelopmental diagnosis has undergone a threefold transformation: it has become demand-led and co-produced rather than professionally imposed, identity-conferring rather than merely descriptive, and self-reinforcing rather than static. The result is a diagnostic culture efficient at conferring diagnoses but weak, unsystematic and largely untheorised in reconsidering them. Drawing on the sociology of diagnosis, labelling theory, Ian Hacking’s account of interactive kinds and discourse-analytic studies of diagnostic contestation, we examine how demand-led medicalisation, the reframing of diagnosis as valued identity and the expansive use of the camouflaging construct can impede revision in practice. Against this background we develop the concept of diagnostic revisability: the capacity of a diagnostic culture to reconsider a diagnostic judgement, in either direction, in the light of change in the person or in the evidence. We distinguish correction of an insecure original judgement, revision in response to change, supersession and reversal of a non-diagnosis, and argue that revisability is an intrinsic property of diagnosis understood as defeasible inference. Precedents exist in medication review and deprescribing and in diagnostic de-labelling elsewhere in medicine. The case is stronger for ADHD, where symptoms and diagnostic status fluctuate and diagnosis is linked to prescribing, than for autism, where it rests principally on the security of the original assessment. Recent Swedish proposals for de-diagnosis services make revisability visible as an object of policy, but the conceptual case does not itself entail support for any service model. Diagnostic revision may correct error; it may also threaten identity, access to support and self-understanding, fall unequally on particular groups, or become a mechanism for rationing. If revisability is translated into practice, it must therefore satisfy stringent ethical and institutional safeguards, including an explicit equity criterion. The design requirements presented are minimum conditions for responsible revision and criteria for when it should not proceed.
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2. Caci H, Caron P. Isolated increased free-triiodothyronine in medication-naïve children and adolescents with ADHD: a retrospective observational study. Front Endocrinol (Lausanne). 2026; 17: 1915311.
BACKGROUND: Thyroid hormones, free triiodothyronine (free-T3) in particular, are crucial for fetal development and child growth and may influence neurodevelopmental disorders including Attention-Deficit/Hyperactivity Disorder (ADHD) in children and adolescents. Yet data are scarce and inconsistent, often relying on adult rather than pediatric reference intervals or on incomplete thyroid panels, and the value of free-T3 as a biomarker across development remains unclear. METHODS: In this retrospective observational study, we characterized thyroid function in medication-naïve patients aged 6 to 17 years with ADHD, using community laboratory results collected between March 2004 and December 2022 in a university pediatric department. Thyroid testing was prescribed prior to methylphenidate initiation. We determined the percentage of patients with free-T3, free-T4, and TSH levels below, within, or above age- and sex-adjusted reference intervals. In the largest immunoassay subgroup (ADVIA Centaur; n = 404), individual free-T3 values were converted to z-scores using published pediatric normative data. A longitudinal ancillary analysis assessed temporal stability in patients with repeat measurements. No non-ADHD comparison group was available. RESULTS: Among 715 medication-naïve patients with ADHD (570 boys, 145 girls) with normal TSH, approximately one-third presented with isolated increased free-T3 concentrations (2IfT3 profile) – 33.68% of boys, 27.59% of girls – the most frequent thyroid anomaly observed. In the ADVIA Centaur subgroup, free-T3 z-scores were higher than the pediatric norms across all age groups, with the largest deviation in boys aged 11-14 years. Among 57 patients with repeat testing (median interval 2.57 years), instability was marked: 53.57% of those initially showing 2IfT3 normalized, while 50% of those initially normal developed 2IfT3. CONCLUSION: Isolated increased free-T3 is frequent in medication-naïve pediatric ADHD and most pronounced in boys aged 11-14 years, but its marked temporal instability precludes its use as a stable biomarker. In the absence of a concurrent non-ADHD comparison group, these findings describe the frequency of this biochemical profile within an ADHD cohort rather than establishing an association with ADHD itself. The 2IfT3 profile may reflect a developmentally and state-dependent neuroendocrine pattern, and warrants prospective study incorporating direct pubertal staging, standardized assay methodology, and appropriate controls.
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3. Glaser M, Dieterich L, Ceslik L, Schickardt Z, Gätzner S, Schmitt L, Oberwinkler H, Reining J, Friedrich M, Hemmen K, Schmitz W, McNeill RV, Kittel-Schneider S, Appelt-Menzel A. Adult ADHD, PARK2 copy number variations and the blood-brain barrier: Culture duration-dependent metabolic alterations in human induced pluripotent stem cell-derived in vitro models. Fluids Barriers CNS. 2026; 23(1).
BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a multifactorial neurodevelopmental disorder in which PARK2 copy number variations (CNVs) constitute a rare genetic risk factor. PARK2 encodes parkin, a key regulator of mitochondrial quality control. Mitochondrial dysfunction is implicated in ADHD pathophysiology and can contribute to blood-brain barrier (BBB) disruption. As BBB disruption remains insufficiently understood in ADHD, this study investigated whether adult ADHD and PARK2 CNVs are accompanied by alterations in BBB phenotype, mitochondrial properties, and cellular metabolism. METHODS: Brain capillary endothelial-like cells (BCECs) were generated using 10 donor-specific human induced pluripotent stem cell (hiPSC) lines from adults with ADHD carrying PARK2 CNVs, alongside PARK2 wild type adults with and without ADHD. BCECs were analyzed at the end of differentiation (day 10) and after prolonged culture (day 17) to assess group-associated phenotypes and culture duration-dependent differences. RESULTS: Across all groups, BCECs showed brain endothelial marker expression, high transendothelial electrical resistance (TEER), and low sodium fluorescein (NaFl) permeability at day 10. After prolonged culture, NaFl permeability remained low, whereas TEER-based barrier integrity declined. Prolonged culture of BCECs reduced glycolytic ATP production rates while increasing mitochondrial ATP production and its relative contribution to total ATP production, reflecting a metabolic shift from glycolysis toward oxidative phosphorylation. Despite decreased total ATP production after prolonged culture, cellular energy status was largely preserved, alongside overall lower intracellular reactive oxygen species (ROS) and mitochondrial membrane potential. At day 10, BCECs from ADHD donors carrying PARK2 duplications displayed greater mitochondrial abundance, the highest basal and oxidative stress-induced intracellular ROS levels, and reduced TEER-based barrier integrity, while at day 17, BCECs from ADHD donors with PARK2 deletions exhibited the least glycolysis-dependent ATP production profile, although absolute mitochondrial ATP production remained comparable between groups. CONCLUSIONS: Prolonged culture was associated with broad, ADHD- and PARK2 genotype-independent metabolic remodeling, whereas mitochondrial and metabolic alterations associated with ADHD and PARK2 CNVs were overall small. This study identifies culture duration as a critical parameter for the characterization of hiPSC-derived BBB in vitro models and supports the feasibility of using donor-specific BCECs at the end of differentiation to investigate BBB-associated mechanisms in adult ADHD and PARK2 CNVs.
